ArticlePloS one2015
The Cardioprotective Effect of Vitamin E (Alpha-Tocopherol) Is Strongly Related to Age and Gender in Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Mitochondria, Sex, and Cardiovascular Disease: A Complex Interplay.International journal of molecular sciences · 2025Review
- Heat shock protein 90 mediates the protective effects of vericiguat on myocardial ischemia/reperfusion injury by inhibiting toll-like receptor 4 and c-Jun N-terminal kinases.Iranian journal of basic medical sciences · 2025Article
- Biochemical Changes in Cardiopulmonary Bypass in Cardiac Surgery: New Insights.Journal of personalized medicine · 2023Review
- Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?International journal of molecular sciences · 2023Review
- Targeting Ferroptosis against Ischemia/Reperfusion Cardiac Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Effects of Cardiac Hypertrophy, Diabetes, Aging, and Pregnancy on the Cardioprotective Effects of Postconditioning in Male and Female Rats.Cardiology research and practice · 2019Article
- Targeting mitochondria for cardiovascular disorders: therapeutic potential and obstacles.Nature reviews. Cardiology · 2019Review
- Triggered activity in atrial myocytes is influenced by NaJournal of molecular and cellular cardiology · 2016Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin E (VitE) only prevented cardiovascular diseases in some patients and the mechanisms remain unknown. VitE levels can be affected by aging and gender. We hypothesize that age and gender can influence VitE's cardioprotective effect. Mice were divided into 4 groups according to age and gender, and each group of mice were divided into a control group and a VitE group. The mice were administered water or VitE for 21 days; Afterward, the cardiac function and myocardial infarct size and cardiomyocyte apoptosis were measured after myocardial ischemia reperfusion(MI/R). VitE may significantly improved cardiac function in young male mice and aged female mice by enhancing ERK1/2 activity and reducing JNK activity. Enhanced expression of HSP90 and Bcl-2 were also seen in young male mice. No changes in cardiac function and cardiac proteins were detected in aged male mice and VitE was even liked to exert a reverse effect in cardiac function in young mice by enhancing JNK activity and reducing Bcl-2 expression. Those effects were in accordance with the changes of myocardial infarction size and cardiomyocyte apoptosis in each group of mice. VitE may reduce MI/R injury by inhibiting cardiomyocyte apoptosis in young male mice and aged female mice but not in aged male mice. VitE was possibly harmful for young female mice, shown as increased cardiomyocyte apoptosis after MI/R. Thus, we speculated that the efficacy of VitE in cardiac protection was associated with age and gender.
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